Abstract
A 29-year-old man who had been on continuous ambulatory peritoneal dialysis (CAPD) since 1987 because of neurogenic bladder, was treated with 1α(OH)D3 (0.25→1.0μg/day) to control hyperparathyroidism for 1 year. During the 1 year of CAPD, he suffered from 4 episodes of persistent peritonitis, resulting in abdominal pain, vomiting and bloody dialysate. After additional 3 episodes of peritonitis, he was transfered to regular hemodialysis because of ultrafiltration failure and loss of urine volume. In addition to ectopic calcification of joints and skin, severe metabolic alkalosis was accelerated at this point.
The patient did not show frequent vomiting and/or diarrhea, and severe calcification of the bowel wall was confirmed by CT. Therefore, the metabolic alkalosis was thought to be caused by hyposecretion of bicarbonate ion in the mucosa of intestines.
This case was similar to previous reports of calcifying peritonitis or peritoneal calcification. The calcification in this case was thought to be caused by the use of dialysate with high osmolality or the administration of high dose vitamin D during persistent peritonitis. To prevent this malignant cycling between ectopic calcification and metabolic alkalosis, inhibition of gastric juice secretion may be an appropriate therapeutic strategy.
